Cancer is mainly due to the abnormal cell lesions or cells with abnormal proliferation. The assembled formation of lumps, we called them Tumor. Tumor can be simply classified into benign and malignant. Generally, benign tumors whose growth is relatively slow, and does not affect the adjacent normal tissue, the risk is non-fatal. However, if benign tumor is formed on the vital parts of the body, surgery can often excise without recurrence. Malignant tumor is more commonly known as “cancer”. Proliferations of cancer cells can not only assemble into amass but also locally invade surrounding tissue and transfer to other part of the body through the circulatory system or the lymphatic system. Therefore, if the cancer is not treated properly, it may lead to death. In recent years, the incidence of cancer rise sustainably which treatment is becoming more important.
Generally, the treatment of cancer can be categorized into three types: surgery, radiation therapy and chemotherapy. Due to the different location of the tumor, and the degree of development of the patient's physical condition, many new experimental therapies have been developed in recent years. For example: gene therapy, molecular targeted therapies, and angiogenic therapy.
In addition, in most organisms, replication and maintenance of telomere length of the ends of chromosomes rely on telomerase. Many studies have pointed out that telomerase is only active in some of the high proliferative capacity cells in human body for example, germ cell, hematopoietic cells, stem cells, immortalized cell and most of the tumor cells. In contrast, normal somatic does not have telomerase activity, so telomeres is gradually shortened with increasing number of cell division, when the telomere is shorter to a certain degree, the cells will stop dividing into the aging phase, eventually dying, this period is called M1 (mortality stage 1).
In M1, if inhibit tumor cells (tumor suppressor gene) gene mutates, such as p53 and Rb, which will stop the aging cells stage and continue cell division, this period is called M2 (mortality stage 2). In this period, telomere length will still shorten due to the non-existence of telomerase activity. Telomeres will not be able to protect the integrity of the ends of chromosomes which lead to chromosomal instability phenomenon. The cells cannot complete the genetic message passing and gradually die. Thus, the M2 period is also known as the crisis period. Most of the cells will die in the M2 period, only a few cells survive due to the telomerase activity, these unrestricted cells are divided continuously and becoming the immortality cells (or cancer cells).
Due to the fact that most normal cells with the telomerase activity did not even exist, and vice versa in almost all human tumor cells has active telomerase, telomerase research in targeted therapy has become many emerging target for the drug target treatment.
Rapid growth or excessive proliferation of cells, due to the need to conduct DNA transcription and translation, the supercoiled structure relative essential often unlock and wound, and therefore is responsible for this aspect of the enzyme—topoisomerases considered a target goal of treatment; mainly use when DNA wraps untie the broken part, so that it can no longer be joined together, to inhibition of rapidly dividing cells, such as cancer cells. For the inhibition of topoisomerase mechanisms, there are basically three forms, a first: Drug first engagement with the DNA fragment, followed by topoisomerase II is bonded to the composite body formed by the drugs and DNA; second: topoisomerase II first engagement with the DNA fragment, and then the drug in combination with topoisomerase II and DNA complexes; last one: the drugs will first engage on topoisomerase II, followed by the complex formed realized with the DNA fragment engaging. Comprehensive three paths, and finally are topoisomerase drugs and DNA fragments will form four complex configuration (ternary complex); while the main mechanism of this effect, by the start of double-stranded DNA topoisomerase role cut off, then the complex topology of the enzyme with drugs stay in the DNA, because the DNA is cut not pick, so when copy conduct this point, will be due to the fracture leaving the enzyme can not be the role of cells discriminant for DNA breakage of leading to cell death.
Overall, the anthracycline cytotoxic has pleiotropic effect, and the inhibition of cell growth seems to be very specific, meaning many drugs such as daunorubicin, doxorubicin and other anthracycline have been widely used as anticancer drugs. However, their clinical uses are limited because of their strong cardiotoxicity tolerance.
Furthermore, the application of first-generation of anthracycline such as doxorubicin and daunorubicin, is like a double-edged sword-like, however, some tumor disease can only be treated by these drugs. After long-term administration, the cardiotoxicity and heart failure is induced. Then, the second-generation of anthracycline such as Epirubicin, Ida neomycin have improved the therapeutic index, but the treatment induced cardiomyopathy crisis have not been eliminated.